ESSENTIAL

OIL SAFETY II
METABOLISM, NEUROTOXICITY,
REPRODUCTIVE TOXICITY

ROBERT TISSERAND

The second of a three part series based on a presentation given at

I Aromn ‘95. The full transcript is published in the Conference

Proceedings. Part Three will appear in the next issue.

I
n Part One 1 outlined the administration not dangerous per se, evidenced by the presence of apiol in
importance of understanding because it does depend on qtrantity. the urine of a person who ingested
essential oil composition; how the Most essential oils are in fact consumed large amounts, 12 days after their last
chemical degradation of essential oils in the form of food flavol:rings, but at dose [D’Aprile, 1928 I. This build-up
could have safety implications, and I relatively low doses compared to those in the body may be good in many
comparrd data on hurrlan and animal used in aromatherapy. The risk is very instances, but it also gives further
toxicity. Part ‘live explores some of the much greater than with drrmal dosag:r, weight to the notion that oral dosing,
issues r-elating the melabolism 01 especially as there is a I-isk of acciclcntal while it can be powerfully therapeutic,
essential oils with theii- safety, potential overdosage which dots not apply to can also be dangerous.
dangers relating to neurotoxicity, and dermal administl-ation. Also, in the In several casts of fatal poisoning
Ihr very diffirulr question of amounts normally given in oral dosage, it was not until the second or third
r-eproductive toxicity. some IO-20 times as mrlch essential oil dose that death ensued. A ‘L-year-old
will enter the bloodstream compared to child was given eight drops of
dcrmal administration. wormseed oil, followed by a similar
dose one week later [Wolf, 19351. The
Excretion second dose proved fdtal. A girl of 19
‘I’he fate of essential oils once they have Essential oils normally take between months died af’ter three one-drop
entered the body is complex, for two orie and five days to be eliminated doses of wormseed oil, 12 hours apart
reasons. Firstly, because each (Table 1). Therefore, if taken orally [&ii Lookeren, 19391. The lowest
component has a separate fate, and so on a daily basis, some blCld-up in the recorded fatal dose of apiol is 0.8 g,
it 110 longer makes sense to speak of body would be expected. This is which wds taken daily for 14 days
the whole oil, one must trace the
destiny of each one of the hundreds of
components. Srcondty, a typical
essential oil component will be
metabotiscd, i.e. chemically changed
while in the body, and in some cases it
will undergo more than one such
change. Some essential oil componenls
are metabolised in the skin, but the
great majority of metabolic change
takes place in the liver.

Routes of administration
The metabolism of essential oil
components may vary according to the
route of administration employed. Oral
[Lowenstein and Ballew, 19581. There asthma. During one severe attack, he potcn’iai risk to those with a low
is little doubt that, if only a single dose wils given ‘half a coffee spoon’ convulsive threshold, i.e. a potential IO
had been taken, all three people (perhaps 15-20 drops?) shortly after have epilepsy which has not yet
would have survived. which he suffered a convulsion. He declared itself. This group could be as
fully recovered after 3 days in hospital. high as 5% of the population [Dr Tim
The second case, an l&year-old Betts, private communication].
girl, drank 30 drops of hyssop oil to Because of the lower lrvels used,
treat a cold. One hour later she exterrral use is much less of a risk, A 1967
Toxicity can affect one, or several orgms, suddenly lost consciousness for 10 review of olfactory stimulation of seizures
and this is sometimes a point of minutes, during which she suffered in epileptics concluded that, ‘Reflex
difference between species. Table 2 lists generaiise d contractions and bit he1 epilepsy caused by scent in the narrowest
how these “specific organ” toxicities are tongue. In the third case a 26-year-old sense of the word is very uncommon. It
normally labelled. A neurotoxic woman took 10 drops of hyssop oil on depends on the degree of oversensitivity
substance is one which has a toxic or each of 2 consecutive days, and of the individual to olfactory stimuli’
destructive effect on nervous tissue. suffered a seizure on the second day (translation from the original German)
Essential oils are only likely to cause [Millet, 19X1]. (Here we see another [Nedbal, 19671. It is very unlikely that
serious physical damage to nervous tissue instance of cumulative oral dosing.) the external use of essential oils w0~ild

in fatal or near-fatal cases of poisoning In the case of hyssop oil we can lead to epileptiform seizures, other than

[Wolf, 19351. A more common result of see, firstly, consistency between animal from a handful of essential oils,
neurotoxicity is convulsions, including hyssop.
and one of rhe most potent
convulsant essential oils is Ketones
hyssop. Hyssop oil is powerfully Essential oils most strongly
neurotoxic, and there are implicated as being
several cases of ingestion of the contrdindicated in epilepsy
oil by humans resulting in and fever are those rich in
epileptiform seiLuI-es. artemisia ketone,
pinocamphone, camphor,

HY=P thujone or pulegone. It is

Hyssop is convulsant because notable that each one of
of its pinoramphonr (40%) thrsr components is a ketone.
and iso-pinocamphonc (30%) Some consider ketones in
content. The coIlvLrlsaIlt general to be highly stimulant
effects of hyssop oil were first researched toxicity and human toxicity. Secondly, to the CNS, and therefore a risk to those
in 1891. Doses of 2.5 mg/kg werr the major components of the oil, prone to epilepsy [Franchomme and
injected into dogs, producing almost pinocamphone and iso-pinocalrlpholie, Eniiel, 19901. However, there is no
immediate epileptiform seizul-es seem to be clearly responsible for the reason to believe that essential oils rich in
[<:adCac and Meunier, 18911. Tests in ncurotoxic action of the oil. other krtones present any danger in
rats found that convulsions appeared for epilepsy. While it mdy be true that all
hyssop oil, at dose levels over 0.13 g/kg; The risks convulsants found in essential oils are
intrdperitoneai pinocamphone was In the only recorded cases where seizures ketones, it does not necessarily follow that
found to be convulsant and lethal to rats have been induced by essential oils, most all ketones found in essential oils are
above 0.05 ml/kg [Millet, 1981; Millet of them apparently in non-epileptics, the convulsants (see table 3).
et al., 19791. Both pinocamphone and oils were taken orally. Hyssop oil most
hyssop oil arc potentially convulsant and definitciy represents a serious risk, and
neurotoxic to laboratory animals [Millet has the potential to rdusr rpiieptiform
et al., 1980]. seizures at oral dosage levels. This There is very good evidence that essential
The amounts of hyssop oil usrd in probably IIIcms that even dcrmal oil components in general are able to
these animal rests were generally high. administration of hyssop oil should be cross the placenta and reach the fetus in
However, there are three reported avoided in those vulnerable to seizures. a human pregnancy. Crossing the
cases of low-dose hyssop oil ingestion The m+jority of people with placenta does not neccssariiy mean that
resulting in epileptiform convulsions epilepsy take medication to suppress there is a risk of toxicity to the fetus; this
[Arditti et al., 19781. The first case was their fits. It is unlikely that this group will depend on the toxicity and the
a G-year-old whose mother frequently would be any more at risk than the plasma concentration of the
gave him 2-3 drops of hyssop oil for his general population. However, there is a roInpOuIld.
Parsley 19281. In pregnant rabbits, abortion of juniper berries have a significant
preparations made from parsley have occurred at dosages of514 g, with severe antifertility effect in rats [Agrawal et al.,
tIeen used to procure abortion for a haemorrhage [Patoir et al., 19361. In 1980; PI-akash et al., 19851. An
great mmy years, and are still in use both types of animal, the dosage is ethanolic extract ofjuniper berries was
today, notably in Italy. Apiol, a majot equivalent to approximately 100-200 gin found to demonstrate both an early
component of most parsley leaf and a human. This is some 2M0 times highrr and a late abortifacient activity in rats
seed oils, is generally held to be [Agrdwal et al., 19801.
responsible for the abortifrtcient An ethanolic extract would
action of parsley, and is also contain some essential oil, but
used in its own right as an there is no ehdence that the
abortitidcient. Data is often essential oil is responsible for
difficult to obldin, paI-tly these effects. Since the oil
because of the legal constitutes only some 1.5% of
implications of patients the raw material, and since all
admitting to illegal abortion, the major components of the
and partly because in some cases essential oil are apparently nom
death follows abortion, and toxic, it seems inconceivable
there is no record of how much that juniper oil could he
apiol was taken. Naturally, the responsible for rhe reproductive
cases which have been rrcorded toxicity noted above.
tend to hc the worst ones, in Nutmeg oil, which is
whirh medical intervention has apparently rlon-a~)ortifacicnt,
been urgently sought. contains nL@fl-pinene, myrccne,
Olit of five cases Ii-om Italy, //&cc-pincnc, terpinen-4-01.
all of whom were between 2 and 7 sabinene and timonene (see
months prrgnant, onr aborted tdblc 4). These S>I,I,?

and later died, one did not abort components constitute son1e
but died, and three aborted and 73% of juniper oil. Thr
survived [D’Aprile, 192X] In the administration of ttp to 0.56
case which did not abort, the g/kg 01. nutmeg oil to pregnant
fetus was found to hr dead. Post- than rhc amount of- apiol causing rodents for 10 consecutive days had no
abortive. vaginal hlrrding, sometimes abortion in humans, and highlights the effect on nidation or on maternal or
profuse, is a feature of these cases. A poor correlation bctwccn animals and fetal survival; no teratogenic effect was
cumlllativr cffcct is apparent, apiol humans in this arrrr observed [NTIS 1972, cited in Opdyke,
being taken daily for between 3 and 8 19761. Myrcenr showed no reproductive
day5 hefore either death or abortion Juniper toxicity when tested on pregnant rdb at
ensued. One of the cases cited had Juniper has frcqucntly been llagged 250 mg/kg, which is equivalent to a
traces of apiol in her urine 12 days after as being contraindicated in human dose of 135 g of juniper oil
the last ingestion. pregnancy [Anon., 1934; I,ist and [Delgado et al., 19931.
The lowest total dose of apiol Hiirhammcr, 1976; Anon., 1983; Nutmeg oil is apparently non-
which inducrd abortion was 0.9 g tdken Duke, 1985; Chandler, 1986; Czygan, abortifacient, so it seems unlikely that
for 8 consecutive days. This is 1987; De Smet et a1.,1993]. A vigorous juniper oil could be.
approximately equivalent to 6 ml of attempt was made to trace the source There are two likely reasons why
parsley leaf oil, hrtwecn 1.5 ml and 6 ml of these contraindications. There is juniper oil acquired a ‘tainted’
of parsleyseed oil, or 5 ml of Indian dill evidence that juniper berries are reputdtion, which has since been
oil. The ineviitable conclusion is that all abortifacient, but there is no quoted and re-quoted. Firstly, there has
of these apiol-rich essential oils present a evidence that juniper oil is undoubtedly been some confusion
very high risk of abortion if taken in oral responsible for this effect. between juniper (/un$~rus commvni.r)
doses, and that extel-nal me would also Most of the above referenced and savin (Junipmu sahina).
SCCITI inadvisable in pregnancy. sources refer to ‘&niper’ generically, One research paper, published in
In animal studies, considerably without specifying a particular 1928, has the sub-heading:
higher dosages of apiol appear to he preparation. None of them refers to ‘Emmenagogue Oils (Pennyroya),
tolerated. In pregnant guinea pigs, what seems to bc the only scientific Tansy and Juniper)‘. In the body of
abortion generally did not occur except basis for the abortifacient activity of the text it later states: ‘The popular
at lethal doses, around 2 g ID’Aptile, juniper. Ethanolic and acetone extrrrrts idea has always been that pennyroyal,
ansy, savin and other oils prodrtcr vulntraire. Nouvelles preuvrs drs I%trrt~~~~:~~iti.~~l~~~~
I’t~c~xi.,7101~2-h. Berlin:
lhortion.’ [Datnow, 192X]. It is ver) propriitb Gpileptisantes de I’essence Springci--Verlag.
,hvioIIs that savin and juniper oils d’hyssop. Hull Accid MGrl 43: 261-264. ?? Lowrnstein, L. and Ballrw, D. H.
have been confused. Any such 0 Chandler, K. F. (1986) An (1958) Fatal acute hacmolytic
confusion would readily explain why inconspicuous but insidious drug. anaemia, throrrlhocytopellic pttrpllra,
uniper oil might have been thought Crlnnrlinrr Char-mawuticnl Journal 119: nephrosis and hepatitis resulting from
If as being dangerous in pregnancy, .X3-566. ingestion of a compound cuntaining
since satin certainly is so. 0 Czygdn, F-C. (1987) Warnung vor apiol. Crlnnrlinn Mrdical A tcocintion
Secondly, if juniper berries are unkritischem Gehrauch \‘011 Journal 78: 195-198.
ihortifacient, and if the component Wacholderhccrcn. Zdcchrift ,fiir 0 Millet. Y. et al. (1979) l?tude
responsible for this is unknown, then zYLJtothPra~ir8: 10. expPi-imentale tlf? propriiteb
,tIspicion could toxiqiies convulaivantes
naturally fall on the des csscnccs de
essential oil. Gin has sauge et d’hysope
;L reputation as an du commerce. Reuzrr
abortifacient, hut d’~lcrtroen~r~hnlog7aphir
again juniper oil is rf de Nwro~~hysiologi~
very unlikely to he Cliniqur 1: 12-l 8.
responsible for Amy ?? Millet. Y. ct
such effects, since the al. (1980) 6tude de
dverage maximum la toxicit d’huiles
concentration of essentielles vigitales
juniper oil in du commerce: esscncc
alcoholic beverages is d’hysope et de saugc.
only 0.006% [Leung, MPdrcine I,6galr,
19801.
It would seem,
I ilbxzdqif!
0
23 ( 1) : 9-2 1.
Millet. Y.
therefore, that there (1981) Toxicity of some
is no reason to regard juniper oil as 0 D’Aprile, F. (1928) essential plant
being hazardous during pregnancy. Studio cliiiico-sprriInenralr oils. Clinical and experimental study.
I:‘.~~~~~inl Oil SuJrt,y, hy Kohert sl~ll’intossica/.ioii~ da apiolo. AIuuzli di Clinicnl Toxicology 18( 12): 1485-l 498
I‘isserancl and Tony Balacs, is Ostrtri& (2 Ginr~ologicr 50: 1204-l 227. 0 Nedhal. ,J. (1967) Der Einlluss
puhlishcd hy Chul-chill Livingstone, 0 Datnow, M. M. (1928) An der Geruchsrei7e auf die
ISBN: 0 443 05260 3. experimental investigation concerning Anfdllshercitschaft der Epilepsie.
toxic abortion produced by chemical Zvit rr,/u$ d;rzneimittd I~‘orfbild
agents. ,Journd o/ Obslrtrics and 61(l): 21-23.
Gyr~rt.ology 35: 693-724. 0 Opdyke, D. LJ. (1976)
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and Co.5mdic:\ 7ixidocg
Antifer-tility effects of fruits of of beta-myI-ccnc in rhr rat. I+& nn~l 14.
Juniperus commimis. f’lulntu Mrdica 39: C;hrnricn/7‘oxi&~,q 31(9): W-6%3. 0 I’atoir, A. et al. (1936) Lc role
98-101. 0 De Smet, I’. A. G. M. et al.(eds) ahortif de l’apiol. Par;.\ MPrlical 3:
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Pharmaceutical Press. 0 Duke, J, A. (1985) Handbook of implantation activity of some
0 Anon. (1983) Llr-ili.t/~ 11rrbul mrdic-inn1 h&s. Boca Raton: CRC Press. indigenous plants in rats. Artn IGuo~~rcrn
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